Varicella, or chickenpox, is an infection caused by the varicella-zoster virus (VZV).

The incidence of chickenpox has drastically decreased with the introduction of routine vaccination in 1996.

Nonetheless, chickenpox is still seen in areas of the world where vaccination is not routine mostly in young children.

In countries with routine vaccination, chickenpox is still seen in immunocompromised patients and the elderly due to waning immunity.

Varicella zoster virus, also called human herpesvirus-3 (HHV-3), is transmitted via aerosolized droplet and initially presents as an upper respiratory infection.

Primary viremia occurs 3 to 4 days after infection followed by a secondary viremia that occurs cyclically over a period of approximately 3 days and results in successive crops of lesions.

The incubation period is 2 weeks (range 10 to 21 days) after contact with an infected person.

Chickenpox often begins with a prodrome of fever, chills, malaise, headache, arthralgia, and myalgia. This prodrome may be very mild or undetectable in young children.

One to two days later, the characteristic lesions begin as red macules, which progress rapidly to form papules that evolve into vesicles and/or pustules that eventually rupture and crust (Fig. 7.14). This entire cycle may occur within 8 to 12 hours.

The eruption typically begins on the face, scalp, and trunk and then spreads to involve the extremities (cephalocaudal spread).

The typical vesicles are superficial and thin-walled, and they are surrounded by an irregular area of erythema, giving them the appearance of “a dewdrop on a rose petal” (Fig. 7.15).

The lesions are usually pruritic.

An enanthem may occur, most commonly on the palate as a vesicle or as shallow erosion.

Lesions characteristically appear in successive crops over 3 to 5 days. Thus, lesions in varying stages of development will be present simultaneously (Fig. 7.16).

Most lesions crust within 1 week and crusts usually fall off within 1 to 3 weeks, depending on the depth of involvement.

Large blisters or hemorrhagic lesions can also be seen.

Scarring is not unusual in uncomplicated varicella and appears as “punched-out” skin lesions on the face (Fig. 7.17) or hypertrophic scars on the trunk (Fig. 7.18).

The diagnosis of varicella is usually straightforward, based on the characteristic presentation and clinical findings.

A Tzanck smear showing characteristic herpesvirus-induced multinucleated giant cells can be helpful in establishing the diagnosis.

Direct immunofluorescence, which uses fluorescent-labeled antibodies to detect VZV in skin cells obtained from the base of active lesions can provide rapid and accurate results.

The scrapings from the base of an active lesion and the vesicle contents can be sent for culture of the VZV virus.

PCR and in situ hybridization on tissue samples of active lesions

Serologic tests include varicella IgM and IgG can also be helpful in confirming the diagnosis.

The most common complication in children is bacterial superinfection with Staphylococcus aureus and Group A beta-hemolytic Streptococcus which will present with fever and localized skin symptoms.

Neurologic complications such as encephalitis, meningoencephalitis, cerebellar ataxia, transverse myelitis, or Guillain-Barré syndrome can rarely occur.

Varicella pneumonia is typically seen as a complication of adult onset varicella and is rare in children.

Pregnant patients who develop varicella in the first trimester have a 2.3% to 4.9% risk of delivering a child with the fetal varicella syndrome, a congenital malformation complex with features such as intrauterine growth retardation, prematurity, cicatricial lesions in a dermatomal distribution, limb paresis and hypoplasia, chorioretinitis, and cataracts.